"Postpartum depression (PPD) is a psychiatric disorder, defined as a subtype of major depressive disorder (MDD). It has been reported that 10–15% women suffer from PPD following childbirth . Although the underlying etiology of postpartum depression remains unknown, the abrupt changes in reproductive hormones that women undergo in post-delivery period may cause postpartum depression . "
[Show abstract][Hide abstract] ABSTRACT: Postpartum depression (PPD) is a psychiatric disorder that occurs in 10-15% of childbearing women. It is hypothesized that omega-3 fatty acids, which are components of fish oil, may attenuate depression symptoms. In order to examine this hypothesis, the animal model of postpartum depression was established in the present study. Ovariectomized female rats underwent hormone-simulated pregnancy (HSP) regimen and received progesterone and estradiol benzoate or vehicle for 23 days, mimicking the actual rat's pregnancy. The days after hormone termination were considered as the postpartum period. Forced feeding of menhaden fish oil, as a source of omega-3, with three doses of 1, 3, and 9g/kg/d, fluoxetine 15mg/kg/d, and distilled water 2ml/d per rat started in five postpartum-induced and one vehicle group on postpartum day 1 and continued for 15 consecutive days. On postpartum day 15, all groups were tested in the forced swimming test (FST) and open field test (OFT), followed by a biochemical assay. Results showed that the postpartum-induced rats not treated with menhaden fish oil, exhibited an increase in immobility time seen in FST, hippocampal concentration of corticosterone and plasmatic level of corticosterone, and pro-inflammatory cytokines. These depression-related effects were attenuated by supplementation of menhaden fish oil with doses of 3 and 9g/kg. Moreover, results of rats supplemented with menhaden fish oil were comparable to rats treated with the clinically effective antidepressant, fluoxetine. Taken together, these results suggest that menhaden fish oil, rich in omega-3, exerts beneficial effect on postpartum depression and decreases the biomarkers related to depression such as corticosterone and pro-inflammatory cytokines.
Behavioural Brain Research 05/2014; 271. DOI:10.1016/j.bbr.2014.05.036 · 3.39 Impact Factor
"The postpartum period can therefore be considered a time of readjustment by the HPA axis to placental CRH withdrawal (Hochberg, Pacak, & Chrousos, 2003). Abnormally high levels of pCRH in pregnancy, followed by their subsequent, precipitous withdrawal, have been hypothesized to trigger postpartum depression in vulnerable individuals (Chrousos et al., 1998; Halbreich, 2005; Hochberg et al., 2003; Magiakou et al., 1996; Vitoratos, Papatheodorou, Kalantaridou, & Mastorakos, 2006). Despite the wider literature linking HPA axis dysregulation to depression in the nonpregnant state, only a few studies have investigated whether pCRH shifts during pregnancy pose a risk factor for postpartum depression. "
[Show abstract][Hide abstract] ABSTRACT: Three decades of research point to both biological and psychological risk factors for postpartum depression, but very little research integrates the two. This study bridged this gap by testing whether prenatal social support predicted depressive symptoms at 8 weeks postpartum in a multiethnic sample of 210 women and whether the stress hormone placental corticotropin-releasing hormone (pCRH), measured at 19, 29, and 37 weeks' gestation, mediated this relationship. We found that prenatal family support predicted significantly fewer depressive symptoms postpartum and more gradual increases in pCRH from 29 to 37 weeks' gestation. Furthermore, steeper increases in pCRH during this same period predicted more depressive symptoms postpartum. Finally, these changes in pCRH in late pregnancy mediated the relationship between prenatal family support and postpartum depressive symptoms. These results suggest that social and biological risk factors for postpartum depressive symptoms are intertwined and move us closer to an integrated biopsychosocial understanding of postpartum depression.
"Cultural influences may also affect the severity of postpartum depression as well as contribute to the alleviate symptomatology. Psychosocial characteristics such as marital status (Warner et al. 1996), lack of marriage emotional support (Halbreich 2005), financial, occupational, and family problems (Halbreich 2005; Boyce 2003) increase the risk of PPD. There are also evidences coming from family (Murphy-Eberenz et al. 2006; Forty et al. 2006) and twin studies (Treloar et al. 1999) showing that PPD can be a heritable and at least in subset group, genetically determined. "
[Show abstract][Hide abstract] ABSTRACT: Postpartum depression disorder (PPD) is a severe illness affecting around 15% of deliveries. Several evidences suggest that PPD is, at least, partially genetic determined. The gene encoding BDNF is a strong candidate for pathogenesis of PPD since that it has been observed decrease of serum BDNF in patients suffering from PPD. The gene encoding BDNF has a polymorphism (Val66Met) that alters the regulated protein secretion; the methionine variant being associated with insufficient secretion compared with the Valine variant. We hypothesized that BDNF gene Val66Met polymorphism could be associated with PPD. We assessed 227 subjects randomly selected who had delivery at a maternity hospital using EPDS. Differences in genotype frequency were calculated by chi (2) test. Logistic Regression Analyses was performed to verify the existence of interaction between biological, psychiatric and environmental variables and PPD. Difference between groups was tested with Student's t test. Tests were two-tailed and results significant when p < or = 0.05. No difference in BDNF genotype distribution was observed between the depressed and non-depressed women. Educational level, stress during pregnancy, bipolar disorder and anxiety was strongly associated with PPD. We were not able to show an association between BDNF polymorphisms and PPD. Further studies are necessary to both of confirm our results and improve validity of PPD diagnosis.
Archives of Women s Mental Health 02/2010; 13(3):285-9. DOI:10.1007/s00737-010-0146-6 · 1.96 Impact Factor
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